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Cardiac output and its regional distribution were studied in conscious rats with acute 24-hour streptozotocin (STZ)-induced diabetes using the labeled microsphere technique. Rats were made diabetic with a single intravenous injection of STZ (60 mg/kg). One day post-STZ all rats were divided into two groups in accordance with the results of urine analysis: rats with ketonuria (n = 6) and rats without ketonuria (n = 7). All the experimental animals had similar blood glucose concentration 24 hours after STZ-injection: 408 +/- 15 and 421 +/- 16 mg/100 ml in rats with and without ketonuria, respectively. All STZ-treated rats showed significant alterations in the systemic hemodynamics one day post-STZ. They included a slight hypotension, a decrease in the total peripheral resistance (TPR) and an increase in the cardiac index (CI) and stroke volume (SV) compared to pre-injection level. Rats with ketonuria showed more prominent decrease in TPR (57 +/- 6 vs. 38 +/- 4% in rats without ketonuria, p < 0.05) and more prominent increase in CI (102 +/- 18 vs. 41 +/- 8% in rats without ketonuria, p < 0.05) and SV (105 +/- 19 vs. 32 +/- 10% in rats without ketonuria, p < 0.05). In both experimental groups the blood flow was significantly increased in the small intestine, heart, brain and kidneys compared to preinjection level. Additionally, rats with ketonuria had increased blood flow in the skin and skeletal muscle (by 0.076 +/- 0.019 and 0.056 +/- 0.020 ml/min/g, respectively, p < 0.05).

The hemodynamic effect of combined V2/V1 arginine vasopressin (AVP) antagonist in conscious rats with acute 24 hour streptozotocin (STZ)--induced diabetes was studied using the microsphere technique. The rats were made diabetic with a single intravenous injection of STZ (60 mg/kg). One day after STZ administration the hemodynamic parameters in the experimental animals were measured before and 10 minutes after AVP antagonist injection (50 mg/kg, i.v.). The hemodynamic alterations observed post-antagonist included: 1) an increase in the total peripheral resistance (1.84 +/- 0.15 vs. 1.31 +/- 0.12 mm Hg/ml/min per 100 g before antagonist administration, p < 0.05), 2) a decrease in the cardiac index (49.0 +/- 3.1 vs. 68.7 +/- 5.2 ml/min/100 g before antagonist administration, p < 0.05) and stroke volume (0.40 +/- 0.03 vs. 0.57 +/- 0.06 ml before antagonist administration, p < 0.05), 3) a significant (p < 0.05) decrease in the blood flow to the skin, skeletal muscle, stomach, small intestine and kidneys. The mean arterial pressure and heart rate remained unchangeable post-antagonist. These data suggest that AVP is responsible, at least in part, for prominent hemodynamic alterations observed in conscious rats with 24 hour STZ-induced diabetes.

Effects of intracoronary infused (2 pM/kg/min for 5 min) endothelin-I on coronary blood flow was studied using modification of the method of Vetterlein and Schmidt. Blood flow in extracorporeal circuit was measured by 20 MHz pulsed Doppler flowmeter. One end of the circuit was connected to the left common carotid artery and the other was connected to the especially curved glass cannule which was placed to the origin of the coronary artery and through the right common carotid artery. Five-minute infusion of endothelin was followed by transitory dilatation and then by constriction of coronary vessels. Blockade of dihydropyridine-sensitive Ca-channels potentiated endothelin-induced vasodilation and decreased the constrictor response three-fold.

The effect of acute streptozotocin-induced diabetes mellitus on the systemic hemodynamic parameters was studied in conscious rats by thermodilution technique. Male Wistar rats were made diabetic with a single intravenous injection of streptozotocin (STZ, 50 mg/kg). The most important finding of this work was the elucidation of the systemic vasodilation and increased cardiac index one day after STZ injection. Such alteration in hemodynamic parameters could result in the increased blood flow and capillary hypertension in some vascular beds and, therefore, be considered as a pathogenic factor in the development of diabetic microangiopathy.

The effect of sympathomimetic tyramine on the systemic and regional hemodynamic parameters was studied by the radioactive microsphere technique in experiments on conscious streptozotocin-diabetic and age-matched control rats. The dose of tyramine required for blood pressure elevation on 15-20 mm Hg was 5.6 times as large in diabetic rats as compared to control animals. It was suggested that sympathetic neuropathy may play the role in the development of the cardiovascular alterations in streptozotocin-diabetic rats.

The response to acetylcholine (10(-5) g/ml) was studied on the rat tail artery perfused with Krebs buffer. Perfusion with acetylcholine produced vasodilation (by 69%) in arteries pre-constricted with transmural nerve stimulation. Atropine (10(-6) g/ml) blocked more than 95% of this response. Acetylcholine had a vasodilating effect on arteries pre-constricted with norepinephrine.

Neuromediated behaviour of feline caudal femoral arteries was studied in vitro. Transmural stimulation of arteries, previously constricted by noradrenaline, caused an up to 58% relaxation of the induced tone. Atropine (10(-5) g/ml) blocked this response by 93%. The removal of endothelium did not affect the magnitude of the response. It is suggested that the caudal femoral artery is an example of a blood vessel which has muscarinic receptors located directly on its smooth muscles.